A study published on March 26 in PLoS Pathogens descibes a protein, called VP16, which acts as the gatekeeper for the damaging, infective activity of the herpes virus. Mice were infected with herpes virus carrying a mutated, inactive form of VP16. After the initial infection had faded, the researchers stressed the mice by raising body temperature and watched to see how many mice had a recurrence of a viral outbreak. Stress did not reactivate the virus in these mice.
But in mice infected with herpes carrying the functional form of VP16 did come back, suggesting that VP16 is the key to reactivation.
In addition to pinpointing VP16 as a key player in reawakening the virus, the new study also shows that the VP16 gene becomes active much earlier in the reactivation than in the initial infection. The VP16 protein is made by the active gene in a small number of neurons, which is enough to begin the cascade of infectivity anew. “This paper comes back to say VP16 is the first triggering event,” Triezenberg says.